TripleHelix - ben

[ArchivalUser]

Could you post info about mx of Ventricular Arrythmias from CMDT as you did for Afib previously, it cleared up many things

Would reaaly apprecaite it whenever you have the Time
thx

[ArchivalUser]

Here you go, BEN. from CMDT, 2007


Ventricular Premature Beats (Ventricular Extrasystoles)
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Ventricular premature beats are characterized by wide QRS complexes that differ in morphology from the patient's normal beats. They are usually not preceded by a P wave, although retrograde ventriculoatrial conduction may occur. Unless the latter is present, there is a fully compensatory pause (ie, without change in the PP interval). Bigeminy and trigeminy are arrhythmias in which every second or third beat is premature; these patterns confirm a reentry mechanism for the ectopic beat (see ECG). Exercise generally abolishes premature beats in normal hearts, and the rhythm becomes regular. The patient may or may not sense the irregular beat, usually as a skipped beat. Ambulatory ECG monitoring or monitoring during graded exercise may reveal more frequent and complex ventricular premature beats than occur in a single routine ECG. An increased frequency of ventricular premature beats during exercise is associated with a higher risk of cardiovascular mortality, though there is no evidence that specific therapy has a role.

Sudden death occurs more frequently (presumably as a result of ventricular fibrillation) when ventricular premature beats occur in the presence of organic heart disease but not in individuals with no known cardiac disease (see ECG). If no associated cardiac disease is present and if the ectopic beats are asymptomatic, no therapy is indicated. If they are frequent, electrolyte abnormalities (especially hypokalemia or hyperkalemia and hypomagnesemia), hyperthyroidism, and occult heart disease should be excluded. Pharmacologic treatment is indicated only for patients who are symptomatic. Because of concerns about worsening arrhythmia and sudden death with most antiarrhythmic agents, -blockers are the agents of first choice. If the underlying condition is mitral prolapse, hypertrophic cardiomyopathy, LVH, or coronary disease”or if the QT interval is prolonged”-blocker therapy is appropriate. The class I and III agents (see Table 10“8) are all effective in reducing ventricular premature beats but often cause side effects and may exacerbate serious arrhythmias in 5“20% of patients. Therefore, every attempt should be made to avoid using class I or III antiarrhythmic agents in patients without symptoms.

Ventricular Tachycardia
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Ventricular tachycardia is defined as three or more consecutive ventricular premature beats. The usual rate is 160“240 beats/min and is moderately regular but less so than atrial tachycardia (see ECG). The distinction from aberrant conduction of supraventricular tachycardia may be difficult. The usual mechanism is reentry, but abnormally triggered rhythms occur. Ventricular tachycardia is either nonsustained (lasting less than 30 seconds) or sustained. It may be asymptomatic or associated with syncope or milder symptoms of impaired cerebral perfusion.

Ventricular tachycardia is a frequent complication of acute myocardial infarction and dilated cardiomyopathy but may occur in chronic coronary disease, hypertrophic cardiomyopathy, mitral valve prolapse, myocarditis, and in most other forms of myocardial disease. Torsades de pointes, a form of ventricular tachycardia in which QRS morphology twists around the baseline, may occur spontaneously in the setting of hypokalemia or hypomagnesemia or after any drug that prolongs the QT interval; it has a particularly poor prognosis (see ECG). In nonacute settings, most patients with ventricular tachycardia have known or easily detectable cardiac disease, and the finding of ventricular tachycardia is an unfavorable prognostic sign

Treatment

Acute Ventricular Tachycardia

The treatment of acute ventricular tachycardia is determined by the degree of hemodynamic compromise and the duration of the arrhythmia. The management of ventricular tachycardia in acute infarction has been discussed. In other patients, if ventricular tachycardia causes hypotension, heart failure, or myocardial ischemia, synchronized DC cardioversion with 100“360 J should be performed immediately. If the patient is tolerating the rhythm, lidocaine, 1 mg/kg as an intravenous bolus injection, or amiodarone 150 mg as a slow intravenous bolus over 10 minutes, followed by a slow infusion of 1 mg/min for 6 hours and then a maintenance infusion of 0.5 mg/min for an additional 18“42 hours can be used. If the ventricular tachycardia recurs, supplemental amiodarone infusions of 150 mg over 10 minutes can be given. If the patient is stable, intravenous procainamide, 20 mg/min intravenously (up to 1000 mg), followed by an infusion of 20“80 mcg/kg/min could also be tried. Empiric magnesium replacement (1 g intravenously) may help. Ventricular tachycardia can also be terminated by ventricular overdrive pacing, and this approach is useful when the rhythm is recurrent.

Chronic Recurrent Ventricular Tachycardia

Sustained ventricular tachycardia

Patients with symptomatic or sustained ventricular tachycardia in the absence of a reversible precipitating cause (acute myocardial infarction or ischemia, electrolyte imbalance, drug toxicity, etc) are at high risk for recurrence. In those with significant LV dysfunction, subsequent sudden death is common. Several trials, including the Antiarrhythmic Drug Versus Implantable Defibrillator (AVID) and the Canadian Implantable Defibrillator trials, strongly suggest that these patients should be managed with implantable cardioverter-defibrillator devices (ICDs). In those with preserved LV function, the mortality rate is lower and the etiology is often different than in those with depressed ventricular function. Treatment with amiodarone, optimally in combination with a -blocker, may be adequate. Sotalol may be an alternative, though there is less supporting evidence. However, many times if ventricular tachycardia occurs in a patient with preserved ventricular function, it is either an outflow tract tachycardia or a fascicular ventricular tachycardia, and these arrhythmias will often respond to AV nodal blockers and can be effectively treated with catheter ablation. The role of electrophysiologic studies in this group is less clear than was previously thought, but they may help identify patients who are candidates for radiofrequency ablation of a ventricular tachycardia focus. This is particularly the case for arrhythmias that originate in the RV outflow tract (appearing as left bundle branch block with inferior axis on the surface ECG), the posterior fascicle (right bundle branch block, superior axis morphology), or sustained bundle branch reentry. Catheter ablation can be used as a palliative therapy for those patients with recurrent tachycardia who receive ICD shocks despite antiarrhythmic therapy.

Nonsustained ventricular tachycardia (NSVT)

NSVT is defined as runs of three or more ventricular beats lasting less than 30 seconds. These may be symptomatic (usually experienced as light-headedness) or asymptomatic. In individuals without heart disease, NSVT is not clearly associated with a poor prognosis. However, in patients with structural heart disease, particularly when they have reduced EFs, there is an increased risk of subsequent symptomatic ventricular tachycardia or sudden death. -Blockers reduce these risks in patients who have coronary disease with significant LV systolic dysfunction (EFs < 35“40%), but if sustained ventricular tachycardia has been induced during electrophysiologic testing, an implantable defibrillator may be indicated. In patients with chronic heart failure and reduced EFs”whether due to coronary disease or primary cardiomyopathy and regardless of the presence of asymptomatic ventricular arrhythmias”-blockers reduce the incidence of sudden death by 40“50% and should be routine therapy (see section on Heart Failure).

Although there are no definitive data with amiodarone in this group, trends from a number of studies suggest that it may be beneficial. Other antiarrhythmic agents should generally be avoided because their proarrhythmic risk appears to outweigh any benefit, even in patients with inducible arrhythmias that are successfully suppressed in the electrophysiology laboratory.

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Ventricular Fibrillation & Sudden Death
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Sudden cardiac death is defined as unexpected nontraumatic death in clinically well or stable patients who die within 1 hour after onset of symptoms. The causative rhythm in most cases is ventricular fibrillation, which is usually preceded by ventricular tachycardia except in the setting of acute ischemia or infarction (see ECG). Complete heart block and sinus node arrest may also cause sudden death. A disproportionate number of sudden deaths occur in the early morning hours. Over 75% of victims of sudden cardiac death have severe CAD. Many have old infarctions. Sudden death may be the initial manifestation of coronary disease in up to 20% of patients and accounts for approximately 50% of deaths from coronary disease. When ventricular fibrillation occurs in the initial 24 hours after infarction, long-term management is no different from that of other patients with acute infarction. Other conditions that predispose to sudden death include severe LVH, hypertrophic cardiomyopathy, congestive cardiomyopathy, aortic stenosis, pulmonary stenosis, primary pulmonary hypertension, cyanotic congenital heart disease, atrial myxoma, mitral valve prolapse, hypoxia, electrolyte abnormalities, prolonged QT interval syndrome, the Brugada syndrome and conduction system disease. Late potentials (after the QRS complex) on a signal-averaged surface ECG in patients with prior myocardial infarction may identify a group of patients at risk for ventricular arrhythmias and sudden death.

Unless ventricular fibrillation occurred shortly after myocardial infarction, is associated with ischemia, or is seen with an unusual correctable process (such as an electrolyte abnormality, drug toxicity, or aortic stenosis), surviving patients require evaluation and intervention since recurrences are frequent. Exercise testing or coronary arteriography should be performed to exclude coronary disease as the underlying cause, since revascularization may prevent recurrence. Conduction disturbances should be managed as described in the next section. If prodromal supraventricular arrhythmias or ventricular arrhythmias, such as sustained or nonsustained ventricular tachycardia, are found by ambulatory ECG monitoring, their elimination by pharmacologic therapy or ablation may prevent further episodes. There is growing consensus that if myocardial infarction or ischemia, other precipitating causes of ventricular fibrillation, or bradyarrhythmias and conduction disturbances are not found to be the cause of the sudden death episode, an implantable defibrillator is the treatment of choice for appropriate patients. In addition, evidence from the MADIT II study and Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) suggest that patients with severe LV dysfunction”whether due to an ischemic cause such as a remote myocardial infarction or a nonischemic cause of advanced heart failure”have a reduced risk of death with the prophylactic implantation of a implantable cardioverter-defibrillator. However, there is also evidence that implanting prophylactic ICDs in patients early after myocardial infarction is associated with a trend toward worse outcomes.


Long QT syndrome
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Congenital long QT syndrome is an uncommon disease that is characterized by recurrent syncope, a long QT interval (usually 0.5“0.7 second), documented ventricular arrhythmias, and sudden death. It may occur in the presence (Jervell syndrome, Lange-Nielsen syndrome) or absence (Romano-Ward syndrome) of congenital deafness. Inheritance may be autosomal recessive or autosomal dominant (Romano-Ward). Specific genetic mutations affecting membrane potassium and sodium channels have been identified and help delineate the mechanisms of susceptibility to arrhythmia.

Because this is a primary electrical disorder, usually with no evidence of structural heart disease or LV dysfunction, the long-term prognosis is excellent if arrhythmia is controlled. Long-term treatment with -blockers, permanent pacing, or left cervicothoracic sympathectomy is frequently effective. ICD implantation is recommended for patients in whom recurrent syncope, sustained ventricular arrhythmias, or sudden cardiac death occurs despite drug therapy. The ICD should be considered as primary therapy in certain patients, such as those in whom aborted sudden cardiac death is the initial presentation of the long-QT syndrome, when there is a strong family history of sudden cardiac death, or when compliance or intolerance to drugs is a concern.

Acquired long QT interval secondary to use of antiarrhythmic agents or antidepressant drugs, electrolyte abnormalities, myocardial ischemia, or significant bradycardia may result in ventricular tachycardia (particularly torsades de pointes, ie, twisting about the baseline into varying QRS morphology) (see ECG). Notably, many drugs that are in some settings effective for the treatment of ventricular arrhythmias prolong the QT interval. Prudence dictates that drug therapy that prolongs the QT interval beyond 500 ms be discontinued.
The management of torsades de pointes differs from that of other forms of ventricular tachycardia. Class I, Ic, or III antiarrhythmics, which prolong the QT interval, should be avoided”or withdrawn immediately if being used (see ECG). Intravenous -blockers may be effective, especially in the congenital form; intravenous magnesium should be given acutely. An effective approach is temporary ventricular or atrial pacing, which can both break and prevent the rhythm.

[ArchivalUser]

thank you so Muuchch!!